Posted by SLS on January 3, 2013, at 22:59:03
In reply to Re: More evidence of inflammation and depression., posted by poser938 on January 3, 2013, at 21:39:41
The major side effect to be aware of is brain swelling. This seems to be relatively rare. Watch for headaches and double-vision.
http://www.webmd.com/brain/brain-swelling-brain-edema-intracranial-pressure?page=2
Below are excerpts from an article regarding minoycline and inflammation. It is technical, but bits and pieces are decipherable. Neuroscientists are serious about this drug.
- Scott
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Does minocycline have antidepressant effect?Chi-Un Pae a,b,*,1 , David M. Marks b, Changsu Han b,c, Ashwin A. Patkar b
14 January 2008
Abstract
Only one-third of patients undergoing monotherapy with an antidepressant achieve remission of their depressive symptoms and gain func- tional recovery. Therefore, further exploration of antidepressant mechanisms of action is important in order to facilitate the development of an- tidepressants with new modes of action. Preclinical and clinical studies have demonstrated that major depression is associated with impaired inflammatory responses and deficient neuroprotection. In this regard, we propose that the second-generation tetracycline minocycline may hold a potential as a new treatment for major depression. Emerging findings in animal and human studies of minocycline reveal that it has antidepressant-like neuroprotective and anti-inflammatory actions, and minocycline has been shown to perform as an antidepressant in an accepted animal model (forced swimming test). Anecdotal evidence supports minocyclines efficacy for augmentation of antidepressants in major depres- sive disorder. The following review describes the evidence supporting the consideration of minocycline as a potential antidepressant. We suggest that minocycline may be particularly helpful in patients with depression and comorbid cognitive impairment, as well as depression associated with organic brain disease. We also describe the antinociceptive effect of minocycline and propose a role for minocycline in the treatment of patients with major depression and prominent somatic discomfort and somatoform spectrum disorders. The lack of clinical studies of minocycline for depression is noted. Further studies of the potential therapeutic mechanism of minocycline and its therapeutic implications for major depression are warranted, and may substantially contribute to the development of newer and more effective antidepressants
3. Possible antidepressant effect of minocycline through anti-inflammatory effect:
A growing body of evidence also suggests that dysregula- tion of inflammatory processes may be a major pathophysio- logical mechanism of major depression (e.g., cytokines play a major role in bridging the nervous and immune systems). Pro-inflammatory agents have been implicated in the patho- genesis of major depression, through their direct effects on neural cells or by modulating neurotransmitters and neuropep- tides [2]. A recent preclinical study showed that stress-induced depressive symptoms in mice were associated with increased hippocampal interleukin-1 (IL-1) and that mice altered by de- letion or antagonism of the IL-1 receptor were not prone to de- pressive symptoms when subjected to stress; the study authors assert that elevated brain IL-1 is linked to depression and that reduction or inhibition of brain IL-1 has potent antidepressant effects [26]. Furthermore, the pro-inflammatory cytokine levels (e.g., TNF-a and IL-1b) were found to be consistently higher in patients with major depression than in controls [3,4], and antidepressants reversed these altered levels, dem- onstrating the immunomodulatory effect of antidepressants (TNF-a and IL-1b directly cause depression in animal models) [2]. Nitric oxide (NO) is another pro-inflammatory agent that has been shown to be increased in patients with major depres- sion, a finding that is reversed by antidepressant treatment [11]. Consistent with a potential antidepressant role, minocy- cline has demonstrated a direct inhibitory effect on the pro-in- flammatory cytokines TNF-a, IL-1b, and NO in a preclinical study. More specifically, minocycline suppressed the hypoxic upregulation of these pro-inflammatory agents in cultured rat microglial and neuronal cells [10].
4. Proven antidepressant effect of minocycline in forced swimming test
A recent study in mice evaluated the potential antidepres- sant activity of minocycline alone or in combination with tra- ditional antidepressant drugs or glutamate receptor antagonists using the time sampling method in the forced swimming test (FST). Minocycline demonstrated antidepressant-like actions in that it reduced immobility by increasing climbing behavior, and a subthreshold dose of minocycline synergized the antide- pressant actions of subthreshold doses of desipramine and glu- tamate receptor antagonists [27]. The FST is one of the most commonly used animal models to evaluate antidepressant ac- tivity, and it is sensitive to all of the major classes of antidepressant drugs [27,28]. Of note, antidepressant drugs with predominantly noradrenaline or dopamine enhancing effects reduce immobility by increasing climbing behavior in the time sampling method in the FST. Conversely, antidepressant drugs with predominantly serotonin enhancing effects reduce immobility by increasing swimming [27,29]. Hence, the finding by Molina-Hernandez and colleagues [27] suggests that minocycline produces antidepressant effects through modification of the noradrenergic system in the brain. Interestingly, minocycline did not synergize the antidepressant-like actions of fluoxetine, indicating that minocycline may not directly impact the serotonergic system [27]. Accordingly, as the authors propose, minocycline may be of use for the augmentation of noradrenergic antidepressant drugs [27].
Some see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1034419
URL: http://www.dr-bob.org/babble/20121231/msgs/1034618.html